Step 1 Repro pharm

Question 1

Leuprolide - mechanism & use

Answer 1

GnRH analog (in “lieu” of GnRH): agonist if pulsatile, antagonist if continuous. For infertility (pulsatile), prostate cancer (continuous; use with flutamide = competitive androgen receptor inhibitor), uterine fibroids

Question 2

Leuprolide - toxicity

Answer 2

Antiandrogen effects, nausea, vomiting. (GnRH analog)

Question 3

Testosterone (methyltestosterone) - mechanism & use

Answer 3

Agonist at androgen receptors. Treatment of hypogonadism; promote 2ary sex characteristics. Stimulates anabolism to promote recovery in BURN or INJURY. Treat ER-positive breast cancer too (exemastane)

Question 4

Testosterone (methyltestosterone) - toxicity

Answer 4

Masculinization in females; decr. intratesticular T in males (feedback inhibition of LH by exogenous T) = gonadal atrophy. Premature closure of epiphyseal plates. Bad for LIPIDS: incr. LDL, decr. HDL.

Question 5

Finasteride - mechanism, use, toxicity

Answer 5

5_-reductase inhibitor; decreases T to DHT conversion. Used for BPH, male pattern baldness. Down side? Promotes breast growth

Question 6

Flutamide - mechanism, use

Answer 6

Nonsteroidal competitive inhibitor of androgens @ testosterone receptor. Used for prostate carcinoma

Question 7

Ketoconazole (repro use) - mechanism, use, toxicity

Answer 7

Inhibits desmolase (cholesterol to androstenedione, which is precursor for estrogen; basically inhibits steroid synthesis). Used for PCOS to prevent hirsutism; side effects = gynecomastia / amenorrhea

Question 8

Spironolactone (repro use) - mechanism, use, toxicity

Answer 8

Inhibits steroid binding. Used for PCOS to prevent hirsutism; side effects = gynecomastia / amenorrhea

Question 9

Estrogens (ethinyl estradiol, DES, menstranol) - mechanism & use

Answer 9

Bind estrogen receptors. Used for hypogonadism, ovarian failure, menstrual abnormalities, hormone replacement in postmenopausal females. Used in men with androgen-dep prostate cancer

Question 10

Estrogens (ethinyl estradiol, DES, menstranol) - toxicity

Answer 10

Increased risk of endometrial cancer. Bleeding in postmenopausal women. Increased risk of THROMBI. DES exposure in utero = baby has incr. risk for clear cell adenocarcinoma of vagina. Contraindicated in ER-pos breast cancer or history of DVT

Question 11

Clomiphene - mechanism, use

Answer 11

SERM. Partial agonist at estrogen receptors in HYPOTHALAMUS = prevent normal feedback inhib. of LH/FSH, increasing pituitary LH/FSH secretion, stimulating ovulation. Treats infertility, PCOS

Question 12

Clomiphene - toxicity

Answer 12

Hot flashes, ovarian enlargement, multiple simultaneous pregnancies, visual disturbances (SERM - agonist @ hypothal E receptors = incr. LH/FSH)

Question 13

Tamoxifen - mechanism, use, toxicity

Answer 13

SERM. Antagonist @ breast (and agonist @ bone); used for ER+ breast cancer (treatment & prevention of recurrence). Toxicity: also agonist @ endometrium; increased endometrial cancer risk

Question 14

Ramoxifen - mechanism, use, toxicity

Answer 14

SERM. Agonist @ bone (and antagonist @ breast); used to reduce bone resorption in osteoporosis. ANTagonist @ endometrium, so no increased endometrial cancer risk.

Question 15

Hormone replacement therapy in menopause - use, mechanism, toxicity

Answer 15

For relief of menopausal sx (hot flashes, vaginal atrophy) and osteoporosis (estrogen decreases osteoclast activity). Unopposed HRT increases risk of endometrial cancer, so add progesterone. May increase CV risk.

Question 16

Anastrozole / exemestane - mechanism, use

Answer 16

Aromatase inhibitors used in postmenopausal women with breast cancer (decrease T to estrogen conversion in periphery, which is major source for postmenopausal women).

Question 17

Progestins - mechanism & use

Answer 17

Bind progesterone receptors, reduce growth / increase vascularization of endometrium. Used in OCP, also in treatment of endometrial cancer, abnormal uterine bleeding.

Question 18

Mifepristone - mechanism & use

Answer 18

RU-486. Competitive inhibitor of progestins @ progesterone receptor. Used with misoprostol (PGE1, induces contractions) to terminate pregnancy.

Question 19

Mifepristone - toxicity

Answer 19

Heavy bleeding, nausea/vomiting/anorexia, abdominal pain. (RU-486 = competitive inhibitor of progestins @ progesterone receptor)

Question 20

OCP - mechanism

Answer 20

Prevent estrogen surge, so LH surge doesn’t occur. Ovulation doesn’t occur as a result

Question 21

OCP - advantages

Answer 21

Reliable (<1% failure), decreases endometrial / ovarian cancer risk (decreased estrogen surge), decreased ectopic pregnancy risk, decreased pelvic infections, regulates menses

Question 22

OCP - disadvantages

Answer 22

Taken daily, no STD protection, INCREASES TGs, depression / wt gain / nausea / HYPERTENSION, causes HYPERCOAGULABLE STATE

Question 23

Dinoprostone - mechanism & use

Answer 23

PGE2 analog; causes cervical dilation & uterine contraction (induces labor!)

Question 24

Ritodrine / terbutaline - mechanism & use

Answer 24

Beta-2 agonists. Relax the uterus, reducing premature uterine contractions (ritodrine allows fetus to “return to dreams” in uterus)

Question 25

Tamsulosin - mechanism & use

Answer 25

_1-antagonist. Used for BPH (inhibits smooth muscle contraction). Specific for _1-A/D receptors (prostate) vs vascular _-1B receptors.

Question 26

Sildenafil, vardenafil - mechanism & use

Answer 26

Phosphodiesterase inhibitors; increase cGMP, smooth mm relaxation in corpus callosum = increased blood flow = erection. For erectile dysfunction.

Question 27

Sildenafil, vardenafil - toxicity

Answer 27

First “Hot & Sweaty”, but then Headache, Heartburn (dyspepsia), Hypotension. Also flushing, impaired blue green color vision (weird!). Hypotension can be LIFE-THREATENING in pts taking NITRATES!